We sought to investigate the efficacy of
arsenic trioxide (
As(2)O(3)) against a human gastric cell line implanted in nude mice in vivo, as well as the mechanism involved. The solid
tumor model was created in nude mice with the
gastric cancer cell line SGC-7901. The animals were randomly divided into three groups.
As(2)O(3) was injected into animals in two
arsenic-treated groups (2.5 mg/kg and 5 mg/kg), and the same volume of
saline solution was injected into the control group. The inhibitory effect was observed in every group. Apoptotic cells and apoptotic bodies were observed by transmission electron microscope; the fraction of apoptotic cells was detected by TUNEL (
terminal deoxynucleotidyl transferase dUTP nick-end labeling) under
laser confocal technology. The expression of Fas and FasL was detected by immunohistochemical staining. In nude mice,
after treatment with 5 mg/kg and 2.5 mg/kg
As(2)O(3), approximately 50% and 30%
tumor growth inhibition were observed, respectively (P < 0.05 for both treatment groups). Increase in apoptotic cells and apoptotic bodies appeared in As(2)O(3)-treated
tumors compared with the control group. The fluorescence intensity levels of apoptotic cells in
tumor were significantly higher in the
arsenic-treated groups (P < 0.05 for both treatment groups). The fluorescence intensity level of apoptotic cells in the 5-mg/kg group was higher than that in the 2.5-mg/kg group (P < 0.05). The expression of Fas
protein increased in dose- and time-dependent manner after the treatment with
As(2)O(3), but that of
FasL protein showed no significant difference between control and treated groups.
As(2)O(3) did not induce hepatic and renal system injury in the nude mice.
As(2)O(3) can inhibit the growth of human gastric cell implanted
tumor. We ascribe this to upregulation of Fas, which can induce apoptosis of gastric cells.